We use the zebrafish as an experimental system, working toward two broad research goals: to uncover conserved basic mechanisms that regulate the generation and organization of tissues in the vertebrate embryo and to understand the primary roles of molecular and genetic pathways that are disturbed in birth defects and disease states.

David Grunwald, PhD, is Helen Lowe Bamberger Colby Presidential Endowed Chair of Human Genetics at the University of Utah School of Medicine. He is co-Director of the NIH-sponsored Genetics Training Program, Faculty Advisor of the Mutation Generation and Detection HSC Core Facility, and a member of the Nuclear Control of Cell Growth and Differentiation Program at Huntsman Cancer Institute.

Grunwald earned his BA in Biology from Williams College and his PhD in Genetics from the University of Wisconsin-Madison. He performed postdoctoral studies at the University of Oregon and Princeton University before joining the Department of Human Genetics in 1988. The lab has been supported by March of Dimes, Sloan Foundation, American Cancer Society, Muscular Dystrophy Association, National Science Foundation, and the NIH.


Grunwald’s research team studies cell-intrinsic and as well as intercellular signaling factors that regulate the maintenance or direct the differentiation of tissue precursor cells in the zebrafish. Perturbation of these pathways during embryogenesis underlies birth defects, including a series of congenital myopathies that are modeled in the lab. Perturbation of tissue maintenance and turnover affects regeneration and is a direct contributor to cancer. One project in the lab examines the role of calcium mobilization in Sonic Hedgehog and additional intercellular signaling pathways that instruct tissue patterning and the differentiation of precursor cells. A second project in the lab focuses on the role of the Polymerase Associated Factor-1 transcription factor complex, which we have found is required to maintain the undifferentiated condition of embryonic stem cells. In addition, the lab develops new tools to manipulate the zebrafish genome to advance the study of gene function. Finally, in collaboration with the Jurynec lab, we study familial forms of Osteoarthritis to discover genes associated with susceptibility to OA in people, and work in model organisms to understand the biological processes that govern susceptibility to the disease.

Lab Members

Principal Investigator

David J. Grunwald, Ph.D.



Kazuyuki Hoshijima

Research Associate



Department of Human Genetics
University of Utah
Human Genetics
15 N 2030 E RM 5160
Salt Lake City, Utah 84112-5330







Publications in PubMed

References to Publications:

Hoshijima K, Jurynec MJ, Klatt Shaw D, Jacobi AM, Behlke MA, and Grunwald DJ. (2019). Highly efficient methods for generating deletion mutations and F0 embryos that lack gene function in zebrafish. Developmental Cell, in press.

Chagovetz AA, Ritchie E, Shaw DK, Hoshijima K, and Grunwald DJ. (2019). Interactions among Ryanodine Receptors affect myofiber type development and function. Disease Models and Mechanisms, in press.

Jurynec MJ, Bai X, Bisgrove BW, Jackson H, Nechiporuk A, Palu RAS, Grunwald HA, Su Y-C, Hoshijima K, Yost HJ, and Grunwald DJ. (2019). The Paf1 Complex and P-TEFb function antagonistically to maintain multipotent neural crest progenitors. Development, in press.

Jurynec MJ, Sawitzke AD, Beals TC, Redd MJ, Stevens J, Otterud B, Leppert MH, and Grunwald DJ. (2018). A hyperactivating proinflammatory RIPK2 allele associated with early-onset osteoarthritis. Hum Mol Genet. 27, 2383–2391.

Shaw DK, Gunther D, Jurynec MJ, Chagovetz AA, Ritchie E, and Grunwald DJ. (2018). Intracellular calcium mobilization is required for Sonic hedgehog signaling. Developmental Cell 45, 512-525.

Maxwell AM, Morrow TM, Hoshijima K, Grunwald DJ, and Amacher SL. (2017). tbx6l and tbx16 are redundantly required for posterior paraxial mesoderm formation during zebrafish embryogenesis. Developmental Dynamics, 246, 759-769.

Hoshijima K, Jurynec MJ, and Grunwald DJ. (2016). Precise editing of the zebrafish genome made simple and efficient. Developmental Cell 36, 654-667.